Short-term effects of alcohol consumption

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Results of the 2010 ISCD study ranking the levels of damage caused by drugs, in the opinion of drug-harm experts. When harm to self and others is summed, alcohol was the most harmful of all drugs considered, scoring 72%.

The short-term effects of alcohol (also known formally as ethanol) consumption – due to drinking beer, wine, distilled spirits or other alcoholic beverages – range from a decrease in anxiety and motor skills and euphoria at lower doses to intoxication (drunkenness), stupor, unconsciousness, anterograde amnesia (memory "blackouts"), and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream, it can diffuse into nearly every cell in the body.

The concentration of alcohol in blood is measured via blood alcohol content (BAC). The amount and circumstances of consumption play a large role in determining the extent of intoxication; for example, eating a heavy meal before alcohol consumption causes alcohol to absorb more slowly.[1] The amount of alcohol consumed largely determines the extent of hangovers, although hydration also plays a role. After excessive drinking, stupor and unconsciousness both can occur. Extreme levels of consumption can cause alcohol poisoning and death; in fact, a concentration in the blood stream of 0.40% will kill half of those affected.[2][3] Alcohol may also cause death indirectly, by asphyxiation from vomiting.

Alcohol can greatly exacerbate sleep problems. During abstinence, residual disruptions in sleep regularity and sleep patterns[clarification needed] are the greatest predictors of relapse.[4]

Effects by dosage[edit]

Different concentrations of alcohol in the human body have different effects on the subject.

The following lists the common effects of alcohol on the body, depending on the blood alcohol concentration (BAC).[medical citation needed] However, tolerance varies considerably between individuals, as does individual response to a given dosage; the effects of alcohol differ widely between people. Hence, BAC percentages are just estimates used for illustrative purposes.

Grand Rapids Dip[edit]

Studies suggest that a BAC of 0.01–0.04% would slightly lower the risk, referred to as the Grand Rapids Effect or Grand Rapids Dip,[5][6] based on a seminal research study by Borkenstein, et al.[7] (Robert Frank Borkenstein is well known for inventing the Drunkometer in 1938, and the breathalyzer in 1954.)[8]

Some literature has attributed the Grand Rapids Effect to erroneous data or asserted (without support) that it was possibly due to drivers exerting extra caution at low BAC levels or due to "experience" in drinking. Other explanations are that this effect is at least in part the blocking effect of ethanol excitotoxicity and the effect of alcohol in essential tremor and other movement disorders,[9] but this remains speculative.

Moderate doses[edit]

Ethanol inhibits the ability of glutamate to open the cation channel associated with the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors. Stimulated areas include the cortex, hippocampus, and nucleus accumbens, which are all responsible for both thinking and pleasure seeking. Another one of alcohol's agreeable effects is body relaxation, which is possibly caused by neurons transmitting electrical signals in an alpha waves-pattern; such waves are actually observed (with the aid of EEGs) whenever the body is relaxed.[citation needed]

Short-term effects of alcohol include the risk of injuries, violence, and fetal damage.[10] Alcohol has also been linked with lowered inhibitions, although it is unclear as to what degree this is chemical or psychological as studies with placebos can often duplicate the social effects of alcohol at either low or moderate doses. Some studies have suggested that intoxicated people have much greater control over their behavior than is generally recognized, though they have a reduced ability to evaluate the consequences of their behavior.[11] Behavioral changes associated with drunkenness are, to some degree, contextual.[12][13]

Areas of the brain that are responsible for planning and motor learning are sharpened. A related effect, which is caused by even low levels of alcohol, is the tendency for people to become more animated in speech and movement. This is caused by increased metabolism in areas of the brain associated with movement, such as the nigrostriatal pathway. This causes reward systems in the brain to become more active, which may induce certain individuals to behave in an uncharacteristically loud and cheerful manner.

Alcohol has been known to mitigate the production of antidiuretic hormone, which is a hormone that acts on the kidney to favor water reabsorption in the kidneys during filtration. This occurs because alcohol confuses osmoreceptors in the hypothalamus, which relay osmotic pressure information to the posterior pituitary, the site of antidiuretic hormone release. Alcohol causes the osmoreceptors to signal that there is low osmotic pressure in the blood, which triggers an inhibition of the antidiuretic hormone. As a consequence, one's kidneys are no longer able to reabsorb as much water as they should be absorbing, therefore creating excessive volumes of urine and the subsequent overall dehydration.[citation needed]

Excessive doses[edit]

Acute alcohol intoxication through excessive doses in general causes short- or long-term health effects. NMDA receptors become unresponsive, slowing areas of the brain for which they are responsible. Contributing to this effect is the activity that alcohol induces in the gamma-aminobutyric acid (GABA) system. The GABA system is known to inhibit activity in the brain. GABA could also be responsible for causing the memory impairment that many people experience. It has been asserted that GABA signals interfere with both the registration and the consolidation stages of memory formation. As the GABA system is found in the hippocampus (among other areas in the CNS), which is thought to play a large role in memory formation, this is thought to be possible.

Anterograde amnesia, colloquially referred to as "blacking out", is another symptom of heavy drinking. This is the loss of memory during and after an episode of drinking. When alcohol is consumed at a rapid rate, the point at which most healthy people's long-term memory creation starts failing usually occurs at approximately 0.20% BAC, but it can be reached as low as 0.14% BAC for inexperienced drinkers.

Another classic finding of alcohol intoxication is ataxia, in its appendicular, gait, and truncal forms. Appendicular ataxia results in jerky, uncoordinated movements of the limbs, as if each muscle were working independently from the others. Truncal ataxia results in postural instability; gait instability is manifested as a disorderly, wide-based gait with inconsistent foot positioning. Ataxia causes the observation that drunk people are clumsy, sway back and forth, and often fall down. It is presumed to be due to alcohol's effect on the cerebellum.

Mellanby effect[edit]

The Mellanby effect is the phenomenon that the behavioral impairment due to alcohol is less, at the same BAC, when the BAC is decreasing than when it is increasing.[14] In other words, at a given point on the upward slope of BAC (while drinking), impairment is greater than at a given point on the downward slope (after drinking), even though the BAC is the same at the two points. This effect was confirmed in a 2017 meta-analysis of 26 studies.[15]

Allergic reaction-like symptoms[edit]

Humans metabolize ethanol primarily through NAD+-dependent alcohol dehydrogenase (ADH) class I enzymes (i.e. ADH1A, ADH1B, and ADH1C) to acetaldehyde and then metabolize acetaldehyde primarily by NAD2-dependent aldehyde dehydrogenase 2 (ALDH2) to acetic acid.[16][17] Eastern Asians reportedly have a deficiency in acetaldehyde metabolism in a surprisingly high percentage (approaching 50%) of their populations. The issue has been most thoroughly investigated in native Japanese where persons with a single-nucleotide polymorphism (SNP) variant allele of the ALDH2 gene were found; the variant allele, encodes lysine (lys) instead of glutamic acid (glu) at amino acid 487; this renders the enzyme essentially inactive in metabolizing acetaldehyde to acetic acid.[18][19] The variant allele is variously termed glu487lys, ALDH2*2, and ALDH2*504lys. In the overall Japanese population, about 57% of individuals are homozygous for the normal allele (sometimes termed ALDH2*1), 40% are heterozygous for glu487lys, and 3% are homozygous for glu487lys.[19] Since ALDH2 assembles and functions as a tetramer and since ALDH2 tetramers containing one or more glu487lys proteins are also essentially inactive (i.e. the variant allele behaves as a dominant negative), homozygote individuals for glu487lys have undetectable while heterozygote individuals for glu487lys have little ALDH2 activity.[20] In consequence, Japanese individuals homozygous or, to only a slightly lesser extent, heterozygous for glu487lys metabolize ethanol to acetaldehyde normally but metabolize acetaldehyde poorly and are susceptible to a set of adverse responses to the ingestion of, and sometimes even the fumes from, ethanol and ethanol-containing beverages; these responses include the transient accumulation of acetaldehyde in blood and tissues; facial flushing (i.e. the "oriental flushing syndrome" or Alcohol flush reaction), urticaria, systemic dermatitis, and alcohol-induced respiratory reactions (i.e. rhinitis and, primarily in patients with a history of asthma, mild to moderately bronchoconstriction exacerbations of their asthmatic disease.[21] These allergic reaction-like symptoms, which typically occur within 30–60 minutes of ingesting alcoholic beverages, do not appear to reflect the operation of classical IgE- or T cell-related allergen-induced reactions but rather are due, at least in large part, to the action of acetaldehyde in stimulating tissues to release histamine, the probable evoker of these symptoms.[21][22]

The percentages of glu487lys heterozygous plus homozygous genotypes are about 35% in native Caboclo of Brazil, 30% in Chinese, 28% in Koreans, 11% in Thai people, 7% in Malaysians, 3% in natives of India, 3% in Hungarians, and 1% in Filipinos; percentages are essentially 0 in individuals of Native African descent, Caucasians of Western European descent, Turks, Australian Aborigines, Australians of Western European descent, Swedish Lapps, and Alaskan Eskimos.[23][24] The prevalence of ethanol-induced allergic symptoms in 0 or low levels of glu487lys genotypes commonly ranges above 5%. These "ethanol reactors" may have other gene-based abnormalities that cause the accumulation of acetaldehyde following the ingestion of ethanol or ethanol-containing beverages. For example, the surveyed incidence of self-reported ethanol-induced flushing reactions in Scandinavians living in Copenhagen as well as Australians of European descent is about 16% in individuals homozygous for the "normal" ADH1B gene but runs to ~23% in individuals with the ADH1-Arg48His SNP variant; in vitro, this variant metabolizes ethanol rapidly and in humans, it is proposed, may form acetaldehyde at levels that exceed the capacity of ALDH2 to metabolize.[24][25] Notwithstanding such considerations, experts suggest that the large proportion of alcoholic beverage-induced allergic-like symptoms in populations with a low incidence of the glu487lys genotype reflect true allergic reactions to the natural and/or contaminating allergens particularly those in wines and to a lesser extent beers.[21]


Moderate alcohol consumption and sleep disruptions[edit]

Moderate alcohol consumption 30–60 minutes before sleep, although decreasing, disrupts sleep architecture. Rebound effects occur once the alcohol has been largely metabolized, causing late night disruptions in sleep maintenance. Under conditions of moderate alcohol consumption where blood alcohol levels average 0.06–0.08 percent and decrease 0.01–0.02 percent per hour, an alcohol clearance rate of 4–5 hours would coincide with disruptions in sleep maintenance in the second half of an 8-hour sleep episode. In terms of sleep architecture, moderate doses of alcohol facilitate "rebounds" in rapid eye movement (REM) following suppression in REM and stage 1 sleep in the first half of an 8-hour sleep episode, REM and stage 1 sleep increase well beyond baseline in the second half. Moderate doses of alcohol also very quickly increase slow wave sleep (SWS) in the first half of an 8-hour sleep episode. Enhancements in REM sleep and SWS following moderate alcohol consumption are mediated by reductions in glutamatergic activity by adenosine in the central nervous system. In addition, tolerance to changes in sleep maintenance and sleep architecture develops within 3 days of alcohol consumption before bedtime.

Alcohol consumption and sleep improvements[edit]

Low doses of alcohol (one 360 ml (13 imp fl oz; 12 US fl oz) beer) appear to increase total sleep time and reduce awakening during the night. The sleep-promoting benefits of alcohol dissipate at moderate and higher doses of alcohol.[26] Previous experience with alcohol also influences the extent to which alcohol positively or negatively affects sleep. Under free-choice conditions, in which subjects chose between drinking alcohol or water, inexperienced drinkers were sedated while experienced drinkers were stimulated following alcohol consumption.[27] In insomniacs, moderate doses of alcohol improve sleep maintenance.[28]

Alcohol consumption and fatigue[edit]

Conditions of fatigue correlate positively with increased alcohol consumption.[citation needed]

Alcohol abstinence and sleep disruptions[edit]

Hormonal imbalance and sleep disruptions following withdrawal from chronic alcohol consumption are strong predictors of relapse. During abstinence, recovering alcoholics have attenuated melatonin secretion at onset of a sleep episode, resulting in prolonged sleep onset latencies. Psychiatry and core body temperatures during the sleep period contribute to poor sleep maintenance. The effect of alcohol consumption on the circadian control of human core body temperature is time dependent.

Alcohol consumption and balance[edit]

Alcohol can affect balance by altering the viscosity of the endolymph within the otolithic membrane, the fluid inside the semicircular canals inside the ear. The endolymph surrounds the ampullary cupula which contains hair cells within the semicircular canals. When the head is tilted, the endolymph flows and moves the cupula. The hair cells then bend and send signals to the brain indicating the direction in which the head is tilted. By changing the viscosity of the endolymph to become less dense when alcohol enters the system, the hair cells can move more easily within the ear, which sends the signal to the brain and results in exaggerated and overcompensated movements of body. This can also result in vertigo, or "the spins."[29]


Epidemiology: Disability-adjusted life year for alcohol use disorders per 100,000 inhabitants in 2004.
  no data
  less than 50
  more than 1050

At low or moderate doses, alcohol acts primarily as a positive allosteric modulator of GABAA. Alcohol binds to several different subtypes of GABAA, but not to others. The main subtypes responsible for the subjective effects of alcohol are the α1β3γ2, α5β3γ2, α4β3δ and α6β3δ subtypes, although other subtypes such as α2β3γ2 and α3β3γ2 are also affected. Activation of these receptors causes most of the effects of alcohol such as relaxation and relief from anxiety, sedation, ataxia and increase in appetite and lowering of inhibitions that can cause a tendency toward violence in some people.[30][31][32][33][34][35][36]

Alcohol has a powerful effect on glutamate as well. Alcohol decreases glutamate's ability to bind with NMDA and acts as an antagonist of the NMDA receptor, which plays a critical role in LTP by allowing Ca2+ to enter the cell. These inhibitory effects are thought to be responsible for the "memory blanks" that can occur at levels as low as 0.03% blood level. In addition, reduced glutamate release in the dorsal hippocampus has been linked to spatial memory loss. Chronic alcohol users experience an upregulation of NMDA receptors because the brain is attempting to reestablish homeostasis. When a chronic alcohol user stops drinking for more than 10 hours, apoptosis can occur due to excitotoxicity. The seizures experienced during alcohol abstinence are thought to be a result of this NMDA upregulation. Alteration of NMDA receptor numbers in chronic alcoholics is likely to be responsible for some of the symptoms seen in delirium tremens during severe alcohol withdrawal, such as delirium and hallucinations. Other targets such as sodium channels can also be affected by high doses of alcohol, and alteration in the numbers of these channels in chronic alcoholics is likely to be responsible for as well as other effects such as cardiac arrhythmia. Other targets that are affected by alcohol include cannabinoid, opioid and dopamine receptors, although it is unclear whether alcohol affects these directly or if they are affected by downstream consequences of the GABA/NMDA effects. People with a family history of alcoholism may exhibit genetic differences in the response of their NMDA glutamate receptors as well as the ratios of GABAA subtypes in their brain.[37][38][39][40][41][42][43][44][45][46] Alcohol inhibits sodium-potassium pumps in the cerebellum and this is likely how it corrupts cerebellar computation and body co-ordination.[47][48]

Contrary to popular belief, research suggests that acute exposure to alcohol is not neurotoxic in adults and actually prevents NMDA antagonist-induced neurotoxicity.[49]


Animal models using mammals and invertebrates have been informative in studying the effects of ethanol on not only pharmacokinetics of alcohol but also pharmacodynamics, in particular in the nervous system. Ethanol-induced intoxication is not uncommon in the animal kingdom, as noted here:

"Many of us have noticed that bees or yellow jackets cannot fly well after having drunk the juice of overripe fruits or berries; bears have been seen to stagger and fall down after eating fermented honey; and birds often crash or fly haphazardly while intoxicated on ethanol that occurs naturally as free-floating microorganisms convert vegetable carbohydrates to alcohol."[50]

More recently, studies using animal models have begun to elucidate the effects of ethanol on the nervous system. Traditionally, many studies have been performed in mammals, such as mice, rats, and non-human primates. However, non-mammalian animal models have also been employed; in particular, the Ulrike Heberlein group at UC San Francisco has used Drosophila melanogaster, the fruit fly, taking advantage of its facile genetics to dissect the neural circuits and molecular pathways, upon which ethanol acts. The series of studies carried in the Heberlein lab has identified insulin and its related signaling pathways as well as biogenic amines in the invertebrate nervous system as being important in alcohol tolerance.[51][52][53] The value of antabuse (disulfiram) as a treatment for alcoholism has been tested using another invertebrate animal model, the honey bees.[54] It is important to note that some of the analogous biochemical pathways and neural systems have been known to be important in alcohol's effects on humans, while the possibility that others may also be important remains unknown. Research of alcohol's effects on the nervous system remains a hot topic of research, as scientists inch toward understanding the problem of alcohol addiction.

In addition to the studies carried out in invertebrates, researchers have also used vertebrate animal models to study various effects of ethanol on behaviors.

See also[edit]


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